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It is a double blind randomized clinical trial (Phase 3), aiming to show the superiority of the nebivolol, a third generation β-blocking agent, in comparison with atenolol, a reference β-blocking agent. Nebivolol is a highly β1 selective. It presents the same effects that atenolol on the cardiac frequency and the plod pressure, but us has no noxious effect on the cardiac performance.
the patients, after one month of treatment, have undergone an aorto-coronary by-pass, during which some myocardium samples and mammalian arteries have been taken, which these have been analysed by western blot in order to measure the enzyme eNOS. In the myocardial tissue, no significant statistical difference has been shown between nebivolol (126.92 ± 92.14 u.a. of densitometry in % value of the group atenolol) and atenolol (100.33 ± 24.24 u.a. of densitometry in % values of the group atenolol). This ca be due to the limited number of patients, to variable wealth of the cells expressing eNOS in the various samples, to the pathology of the patient and to his severity. In the mammalian arteries, no signal have been detected at the time of the dosage by western blot, despite repeated essays. The emitted hypotheses are the following: too weak expression of eNOS in the analysed tissues, endothelium destruction, enzyme degradation.
The clinical and hemodynamics parameters, recorded during the trial, have been statistically analysed. Some significant statistical results have been in evidence; the systolic blood pressure is more elevated in the nebivolol group (158.2 ± 22.73 mmHg) than in the atenolol group (123.83 ± 12.09 mmHg), the diastolic blood pressure after one month is lessen in the two group (nebivolol : 81.43 ± 3.78 mmHG versus 68.2 ± 9.62 mmHg ; atenolol : 85 ± 9.26 mmHg versus 66.17 ± 7.88 mmGh).
The trial does not allow to conclude definitively to an absence of nebivolol efficacy on the eNOS expression. Actually, the patient number include is restricted. Furthermore, it is possible than the nebivolol do not rise the tissue expression of the enzyme but increase his production. It would be interesting to investigate the property if the nebivolol in a trial to wider scale Il s’agit d’un essai clinique de phase 3, randomisé en double aveugle, visant à démontrer la supériorité du nébivolol, bêta-boquant de troisième génération, en comparaison avec l’aténolol, bêta-boquant de référence. Le nébivolol est hautement β1 sélectif. Il présente les mêmes effets que l’aténolol sur la fréquence cardiaque et le pression artérielle. Il n’a, par contre, pas d’effets nocifs sur la performance cardiaque.
Les patients, après un mois de traitement, ont subi un pontage aorto-coronaire, aux cours duquel ont été prélevés des échantillons de myocarde et d’artères mammaires, lesquels ont été analysés par western blot afin de doser l’enzyme eNOS. Dans le tissu myocardique, aucune différence statistiquement significative n’a été démontrée entre le nébivolol (126.92 ± 92.14 u.a. de densiométrie en % des valeurs du groupe aténolol) et l’aténolol (100.33 ± 24.24 u.a. de densiométrie en % des valeurs du groupe aténolol). Ceci peut être dû au nombre limité de patients, à la richesse variable des cellules exprimant eNOS dans les divers prélèvements, à a pathologie propre du patient et à sa sévérité. Dans les artères mammaires, aucun signal n’a pu être détecté lors du dosage par western blot, malgré des essais répétés. Les hypothèses émises sont les suivantes : expression trope faible de eNOS au sein des tissus analysés, destruction de l’endothélium, dégradation de l’enzyme.
Outre le dosage de l’enzyme eNOS, ont été analysés statistiquement les paramètres cliniques et hémodynamiques relevés au cours de l’étude. Des résultats statistiquement significatifs ont été mis en évidence ; la pression artérielle systolique au moment de l’induction de l’anesthésie est plus élevé dans le groupe nébivolol (158.2 ± 22.73 mmHg) que dans le groupe aténolol (123.83 ± 12.09 mmHg), la pression artérielle diastolique après un mois de traitement a diminué de manière significative aussi bien dans le bras nébivolol (81.43 ± 3.7 mmHg versus 68.2 ± 9.62 mmHg) que dans le bras aténolol (85 ± 9.26 mmHg versus 66.17 ± 7.88 mmHg).
L’essai ne permet pas de conclure définitivement à une absence d’efficacité du nébivolol sur l’expression de l’enzyme eNOS. En effet, le nombre de patient inclus est restreint. De plus, il est possible que le nébivolol n’augmente pas l’expression tissulaire de l’enzyme mais augmente sa production. Il serait intéressant d’investiguer les propriétés du nébivolol dans un essai à plus large échelle

Atenolol --- Adrenergic Antagonists --- Blood Pressure --- Nitric Oxide Synthase

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Nitric Oxide Synthase --- Gene Expression --- Liver --- ATP-Binding Cassette Transporters --- Endotoxemia --- genetics --- enzymology --- metabolism --- physiopathology

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Nitric Oxide Synthase. --- Chromatography, High Pressure Liquid --- Mass Spectrometry --- Citrulline --- Endothelium, Vascular --- Nitric-Oxide Synthase --- Nitric-Oxide Synthetase --- NO Synthase --- Nitric Oxide Synthetase --- Oxide Synthase, Nitric --- Synthase, Nitric Oxide --- methods. --- blood. --- drug effects. --- Theses --- Hungarian literature --- Nitric Oxide Synthase --- methods --- blood --- drug effects --- 09 <042> --- 02 <041> --- 02 <041> Bibliotheekwezen--Brochures. Pamfletten. Essays --- Bibliotheekwezen--Brochures. Pamfletten. Essays --- 09 <042> Handschriften. Oude en merkwaardige drukken. Curiosa--Redevoeringen. Lezingen. Toespraken --- Handschriften. Oude en merkwaardige drukken. Curiosa--Redevoeringen. Lezingen. Toespraken

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Oxytocin secretion from the posterior pituitary gland is increased during parturition, stimulated by the uterine contractions that forcefully expel the fetuses. Since oxytocin stimulates further contractions of the uterus, which is exquisitely sensitive to oxytocin at the end of pregnancy, a positive feedback loop is activated. The neural pathway that drives oxytocin neurons via a brainstem relay has been partially characterised, and involves A2 noradrenergic cells in the brainstem. Until close to term the responsiveness of oxytocin neurons is restrained by neuroactive steroid metabolites of progesterone that potentiate GABA inhibitory mechanisms. As parturition approaches, and this inhibition fades as progesterone secretion collapses, a central opioid inhibitory mechanism is activated that restrains the excitation of oxytocin cells by brainstem inputs. This opioid restraint is the predominant damper of oxytocin cells before and during parturition, limiting stimulation by extraneous stimuli, and perhaps facilitating optimal spacing of births and economical use of the store of oxytocin accumulated during pregnancy. During parturition, oxytocin cells increase their basal activity, and hence oxytocin secretion increases. In addition, the oxytocin cells discharge a burst of action potentials as each fetus passes through the birth canal. Each burst causes the secretion of a pulse of oxytocin, which sharply increases uterine tone; these bursts depend upon auto-stimulation by oxytocin released from the dendrites of the magnocellular neurons in the supraoptic and paraventricular nuclei. With the exception of the opioid mechanism that emerges to restrain oxytocin cell responsiveness, the behavior of oxytocin cells and their inputs in pregnancy and parturition is explicable from the effects of hormones of pregnancy (relaxin, estrogen, progesterone) on pre-existing mechanisms, leading through relative quiescence at term inter alia to net increase in oxytocin storage, and re

Activation. --- Activity. --- Adaptation. --- Allopregnanolone. --- Behavior. --- Birth. --- Brainstem. --- C-fos expression. --- Dendrites. --- Dynorphin. --- Enkephalin. --- Estrogen receptors. --- Estrogen. --- Feedback. --- Fetuses. --- Firing. --- Gaba. --- Gamma-aminobutyric-acid. --- Gland. --- Hormone. --- Hormones. --- Hypothalamic paraventricular nucleus. --- Increase. --- Increases. --- Inhibition. --- Main olfactory-bulb. --- Mechanisms. --- Messenger-ribonucleic-acid. --- Milk-ejection reflex. --- Neurons in-vitro. --- Neurons. --- Nitric oxide synthase. --- Nitric-oxide synthase. --- Nucleus tractus solitarius. --- Opioid. --- Oxytocin mrna. --- Oxytocin. --- Parturition. --- Pattern. --- Patterns. --- Pituitary. --- Potentials. --- Pregnancy. --- Progesterone-receptor expression. --- Progesterone. --- Rat supraoptic nucleus. --- Response. --- Restraint. --- Review. --- Secretion. --- Steroid metabolites. --- Steroid. --- Stimulation. --- Stimuli. --- Supraoptic nucleus. --- System. --- Time. --- Uterus.

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The papers reported here will contribute to proposing new insights into the mechanisms of several conditions, as well as suggesting new diagnostic alternatives and therapeutic targets in widespread pathologies such inflammation and inflammatory-based diseases. The discovery of the new is, as always, anchored in recourse to the old.

toxicity --- long-lasting effect --- iso-?-acids --- ammonium glycyrrhizinate --- metabolomics --- cytokines --- Alnus sibirica --- energy metabolism --- curcumin --- antineuroinflammation --- nitric oxide --- antioxidant --- nutraceutical food --- liver --- nardochinoid B --- endometriosis --- adipose tissue --- Nardostachys chinensis --- tau --- macrophage --- nociception --- heme oxygenase-1 --- enzymatic hydrolysis --- IL-6 --- nuciferine --- docking --- chronic nonbacterial prostatitis --- black tea polyphenol --- network pharmacology --- Tagetes patula L. --- SEM --- lipopolysaccharide --- solid lipid nanoparticle --- tauopathy --- memory --- lupane-type triterpene --- acute lung injury --- inducible nitric oxide synthase --- inflammation --- anti-inflammatory --- microglia --- resveratrol --- theaflavins --- hirsutanonol --- short-term high-fat diet --- inflammatory disease --- juçara --- oregonin --- PPARs --- NF-?B --- neuroprotection --- Portulaca oleracea --- TNF-? --- depression